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general anaesthesia

traditional stages of anaesthesia

  1. stage of analgesia
    • no amnesia until late in stage.
  2. stage of excitement
    • delirium, excited, amnesic, irregular respiration, vomiting, incontinence.
  3. stage of surgical anaesthesia
    • recurrence of regular respiration;
    • 4 planes described according to pupil size, eye reflexes & ocular movements
    • 4 EEG phases of maintenance anaesthesia:
      • phase 1: light anaesthesia - decrease in EEG beta activity (13-30Hz), increase in alpha activity (8-12Hz) and delta activity (0-4Hz)
      • phase 2: intermediate state - an increase in alpha and delta activity in the anterior leads compared to posterior leads “anteriorization”, and EEG resembles stage 3 non-REM (slow-wave) sleep
      • phase 3: deep anaesthesia - EEG characterised by flat periods interspersed with periods of alpha and delta activity
      • phase 4: profound anaesthesia - EEG is flat, isoelectric and this phase induced by barbiturates or propofol is often used as a neuroprotective function in neurosurgery, or in Mx of status epilepticus.
    • approximates brain-stem death as patients are:
      • unconscious, have depressed brain stem reflexes, do not respond to nociceptive stimuli, have no apnoeic drive
      • require cardiorespiratory and thermoregulatory support
  4. stage of medullary depression
    • severe depression of vasomotor & respiratory centres
    • ⇒ death without full circulatory & resp. support

signs of induction of anaesthesia

  • failure of patient to track movement of your finger with their eyes +/- onset of nystagmus
  • blinking increases
  • oculocephalic, eyelash and corneal reflexes are lost but pupillary light reflex remains
  • heart rate typically increases unless opiates or benzodiapines have been administered prior to or during induction
  • while BP may rise or fall

signs of inadequate general anaesthesia

  • heart rate and/or BP may rise dramatically
  • perspiration
  • tearing
  • changes in pupil size
  • return of muscle tone and movement if not paralysed by muscle relaxants
  • changes in EEG measures of brain activity

mechanism of action of general anaesthetics

  • actual mechanisms are complex
  • it appears many agents act by suppressing neuronal activity in the brain stem arousal centres - the lateral dorsal tegmental areas of the pons and the midbrain paramedian region.
  • apnoea is partly due to actions on GABA[sub]A[/sub] interneurons in the respiratory control network in the ventral medulla and pons.
  • the rapid atonia following a propofol bolus is thought to be due to actions on the spinal cord as well as the pontine and medullary reticular nuclei that control antigravity muscles

pharmacokinetics of inhaled general anaesthetics

  • depth of anaesthesia determined by concentration in CNS.

uptake from lungs & distribution

  • Concentration of a gas is proportional to its partial pressure (tension).
  • Rate at which a given concentration of anaesthetic is achieved in CNS depends upon:
solubility of gas:
  • blood:gas partition coefficient = relative affinity for blood cw air
  • poorly soluble gases (ie. low blood:gas partition coefficient) (eg. N2O):
    • relatively few molecules are needed to diffuse to raise arterial tension
      • ⇒ perfusion limited
      • ⇒ high arterial tensions develop rapidly
      • ⇒ faster induction of anaesthesia
      • ⇒ at equilibrium, arterial tension closer to alveolar tension
      • eg. N2O reaches ~90% of its alveolar tension but methoxyflurane only 20%
anaesthetic blood:gas coefficient brain:blood coefficient MAC
nitrous oxide 0.47 1.1 >100% ie. cannot be used alone for GA
sevoflurane 0.69 1.7 2.0
isoflurane 1.4 2.6 1.4
enflurane 1.8 1.4 1.68
halothane 2.3 2.9 0.75
methoxyflurane 12.0 2.0 0.16
inspired concentration
  • proportional to alveolar tension achieved
    • ⇒ higher concentrations increase rate of rise of arterial tension
    • ⇒ increase rate of induction of GA
    • THUS, use 3-4% halothane initially then maintenance of 1-2%
pulmonary minute ventilation
  • proportional to rate of rise of arterial tension achieved effect greatest on high soluble gases (eg. methoxyflurane, halothane) eg. 4x minute ventilation ⇒ doubles arterial tension of halothane in 1st 10'
pulmonary blood flow
  • increased cardiac output SLOWS rate of rise of arterial tension less time of blood in contact with alveolus larger volume of blood exposed to gas
    • ⇒ shock increases rate of induction esp. for high-soluble drugs
arterio-venous concentration gradient
  • the greater the difference, the longer the time required for equilibration gradient depends on degree of uptake in tissues which depends upon:
    • tissue perfusion (brain,heart,liver,kidneys > muscle > adipose)
    • solubility in that tissue


  • rate of recovery from GA depends on redistribution away from brain & elimination.

elimination by lungs

  • depend on factors as for uptake BUT:
    • while uptake can be increased by increasing inspired concentration, the reverse process cannot be enhanced as cannot reduce conc. below zero.
    • tension in various tissues is variable (ie. not zero as at start of GA) & depends on:
      • solubility in tissues, perfusion of tissues
      • duration of GA - longer duration ⇒ higher tissue tensions ⇒ slower recovery
      • poorly soluble gases are “washed out” faster ⇒ rapid recovery

hepatic metabolism

  • esp. methoxyflurane (→ release of fluoride ions) & halothane (15-20% metabolised).

dose-response characteristics

Minimum Alveolar Concentration (MAC):

  • partial pressure of alveolar gas as a % of 760mmHg that results in immobility in 50% pts when exposed to noxious stimuli such as surgical incision ie. represents the ED50 on a conventional quantal dose-response curve
  • THUS is a measure of relative anaesthetic potency
  • it gives NO information about the slope of this curve, but in general, it is steep ie. >95% pts may fail to respond to surgical incision @ 1.1MAC !!
  • individual pts require between 0.5 - 1.5 MAC for GA
  • MAC values decrease with age but NOT affected by sex, height or weight.
  • MAC values may decrease substantially when adjuvant drugs used (eg. opiates).

effects of inhaled general anaesthetics on organ systems


  • halothane, enflurane
    • ⇒ decreased cardiac output but no effect on total peripheral resistance (TPR) ⇒ decreased BP
    • myocardial depressant effect ⇒ reduced myocardial oxygen needs
  • isoflurane ⇒ marked decrease in TPR but little effect on cardiac output ⇒ decreased BP
  • all GA's tend to increase right atrial pressure (RAP)si
  • GA's alter heart rate via direct effect on no-atrial (SA) node &/or via autonomic effects
  • halothane sensitises myocardium to catecholamines ⇒ risk of ventricular fibrillation (VF)


  • all GA's except N2O decrease tidal volume & increase resp. rate → decreased minute ventilation
  • all GA's
    • ⇒ increase resting PaCO2
    • ⇒ increase apnoeic threshold
    • ⇒ decreased ventilatory response to hypoxia - important in recovery phase where this response needed
    • ⇒ depress mucociliary function → pooling of mucus
    • ⇒ tend to cause bronchodilation


  • all GA's ⇒ decrease metabolic rate of brain
  • most GA's
    • ⇒ increase cerebral blood flow via decreased cerebral vascular resistance
    • ⇒ raised intracranial pressure (least with N2O)
  • NB. although N2O has low GA potency, it has marked analgesic & amnesic effects


  • all GA's
    • ⇒ decreased effective renal blood flow (RBF) & glomerular filtration rate (GFR)
    • ⇒ increased filtration fraction
    • ⇒ increased renal vascular resistance ⇒ impaired autoregulation
  • methoxyflurane ⇒ flouride ions and other metabolites ⇒ irreversible polyuric renal failure


  • all GA's ⇒ decreased hepatic blood flow (15-45% of pre-GA flow)
  • halothane ⇒ possible hepatotoxicity


  • most (not N2O) ⇒ potent uterine muscle relaxation
    • ⇒ helpful in manipulations of fetus during delivery
    • ⇒ risk of haemorrhage in D&C's, etc.


  • N2O ⇒ prolonged exposure causes megaloblastic anaemia


anaestheticsgeneral.txt · Last modified: 2019/06/27 07:35 by

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